Bachmann Kaspar F, Moller Per Werner, Hunziker Lukas, Maggiorini Marco, Berger David
Department of Intensive Care Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
Department of Anesthesia, SV Hospital Group, Institute of Clinical Sciences at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
J Intensive Care. 2024 May 11;12(1):19. doi: 10.1186/s40560-024-00730-6.
To optimize right ventricular-pulmonary coupling during veno-arterial (VA) ECMO weaning, inotropes, vasopressors and/or vasodilators are used to change right ventricular (RV) function (contractility) and pulmonary artery (PA) elastance (afterload). RV-PA coupling is the ratio between right ventricular contractility and pulmonary vascular elastance and as such, is a measure of optimized crosstalk between ventricle and vasculature. Little is known about the physiology of RV-PA coupling during VA ECMO. This study describes adaptive mechanisms for maintaining RV-PA coupling resulting from changing pre- and afterload conditions in VA ECMO.
In 13 pigs, extracorporeal flow was reduced from 4 to 1 L/min at baseline and increased afterload (pulmonary embolism and hypoxic vasoconstriction). Pressure and flow signals estimated right ventricular end-systolic elastance and pulmonary arterial elastance. Linear mixed-effect models estimated the association between conditions and elastance.
At no extracorporeal flow, end-systolic elastance increased from 0.83 [0.66 to 1.00] mmHg/mL at baseline by 0.44 [0.29 to 0.59] mmHg/mL with pulmonary embolism and by 1.36 [1.21 to 1.51] mmHg/mL with hypoxic pulmonary vasoconstriction (p < 0.001). Pulmonary arterial elastance increased from 0.39 [0.30 to 0.49] mmHg/mL at baseline by 0.36 [0.27 to 0.44] mmHg/mL with pulmonary embolism and by 0.75 [0.67 to 0.84] mmHg/mL with hypoxic pulmonary vasoconstriction (p < 0.001). Coupling remained unchanged (2.1 [1.8 to 2.3] mmHg/mL at baseline; - 0.1 [- 0.3 to 0.1] mmHg/mL increase with pulmonary embolism; - 0.2 [- 0.4 to 0.0] mmHg/mL with hypoxic pulmonary vasoconstriction, p > 0.05). Extracorporeal flow did not change coupling (0.0 [- 0.0 to 0.1] per change of 1 L/min, p > 0.05). End-diastolic volume increased with decreasing extracorporeal flow (7.2 [6.6 to 7.8] ml change per 1 L/min, p < 0.001).
The right ventricle dilates with increased preload and increases its contractility in response to afterload changes to maintain ventricular-arterial coupling during VA extracorporeal membrane oxygenation.
为了在静脉 - 动脉（VA）体外膜肺氧合（ECMO）撤机过程中优化右心室 - 肺耦合，常使用正性肌力药、血管升压药和/或血管扩张剂来改变右心室（RV）功能（收缩力）和肺动脉（PA）弹性（后负荷）。右心室 - 肺动脉耦合是右心室收缩力与肺血管弹性之间的比率，因此是心室与血管系统之间优化串扰的一种度量。关于VA ECMO期间右心室 - 肺动脉耦合的生理学知之甚少。本研究描述了在VA ECMO中因前负荷和后负荷条件变化而维持右心室 - 肺动脉耦合的适应性机制。
在13头猪中，在基线时将体外循环流量从4降至1 L/min，并增加后负荷（肺栓塞和低氧性血管收缩）。压力和流量信号用于估计右心室收缩末期弹性和肺动脉弹性。线性混合效应模型估计条件与弹性之间的关联。
在无体外循环流量时，收缩末期弹性从基线时的0.83[0.66至1.00]mmHg/mL增加，肺栓塞时增加0.44[0.29至0.59]mmHg/mL，低氧性肺血管收缩时增加1.36[1.21至1.51]mmHg/mL（p <0.001）。肺动脉弹性从基线时的0.39[0.30至0.49]mmHg/mL增加，肺栓塞时增加0.36[0.27至0.44]mmHg/mL，低氧性肺血管收缩时增加0.75[0.67至0.84]mmHg/mL（p <0.001）。耦合保持不变（基线时为2.1[1.8至2.3]mmHg/mL；肺栓塞时增加 - 0.1[-0.3至0.1]mmHg/mL；低氧性肺血管收缩时增加 - 0.2[-0.4至0.0]mmHg/mL，p>0.05）。体外循环流量未改变耦合（每变化1 L/min为0.0[-0.0至0.1]，p>0.05）。舒张末期容积随着体外循环流量的减少而增加（每1 L/min变化7.2[6.6至7.8]ml，p <0.001）。
在VA体外膜肺氧合期间，右心室随着前负荷增加而扩张，并响应后负荷变化增加其收缩力，以维持心室 - 动脉耦合。
